Sleep Mechanisms Research Articles

388 Familial natural short sleepers have greater resilience than unaffected family members

Abstract Introduction Resilience, a life-long trait, corresponds to the ability to bounce back from adversity. What factors influence resilience is unclear. Here we describe a cohort of individuals with familial natural short sleep (FNSS). Four genes in five families have been identified that confer this trait, DEC2, NPSR1, GRM1 and ADRB1. Individuals in this cohort share a resilience phenotype alongside this decreased sleep need. Methods Those reporting less than 6.5 hours of sleep when allowed to sleep ad libitum without any complaints regarding overnight sleep or daytime sleepiness were then interviewed to determine FNSS affected status from 2009 to 2020. Data on mood, depression, sleepiness and resilience were collected from participants and family members enrolled in the FNSS study. Results 163 individuals meeting criteria for FNSS were enrolled. Compared to 47 unaffected family members, they had significantly shorter sleep duration as measured by self report and actigraphy, significantly more resilience as measured by the Connor-Davidson Resilience Scale, significantly less sleepiness as measured by the Epworth Sleepiness Scale, and significantly fewer symptoms of depression as measured by the Beck Depression Inventory. Conclusion FNSS individuals appear to have a distinct phenotype including shorter sleep duration, greater resilience, less subjective sleepiness, and fewer symptoms of depression. Better understanding the genetics and characteristics of those with familial natural short sleep may provide insight into mechanisms of both restorative sleep and resilience. Support (if any) This work was supported by NIH grants NS099333, NS072360 and NS104782 to L.J.P. and Y-H.F., and by the William Bowes Neurogenetics Fund to L.J.P. and Y.H.F.

663 Improved Sleep After a Brief Intervention for Insomnia Mediates Improvements in Depression Symptoms During the COVID-19 Pandemic

IntroductionThe COVID-19 Pandemic and mitigation efforts have led to drastic increases in acute insomnia symptoms, which left untreated may contribute to increased risk for other negative mental health outcomes, including depression. However, the impact of treating acute insomnia symptoms on future depression outcomes remains unknown. Moreover, whether sleep improvements as a result of an insomnia treatment mediate subsequent reduction of depression symptoms similarly remains unknown.MethodsAt this writing, 44 individuals experiencing insomnia symptoms (Insomnia Severity Index; ISI ≥ 10) that began during the COVID-19 pandemic have been randomized to receive a brief, telehealth Cognitive Behavioral Therapy for Insomnia (CBTI) waitlist control. Treatment was delivered in 4 sessions over a 5-week period. CBTI is the gold-standard behavioral intervention for chronic insomnia and has been applied successfully via telemedicine. Outcome measures were depressive symptoms as measured by the Patient Health Questionnare-9 (PHQ-9) minus the sleep item and insomnia symptom severity as measured by the ISI. Both outcome measures were collected at baseline (week 0), throughout treatment phase (weeks 2–6), and at the post-treatment (week 7). Linear mixed models determined the impact of treatment on depression and insomnia symptom severity. Mediation was tested using the MacArthur framework.ResultsThere was a significant Group x Time interaction, with CBTI leading to a greater rate of improvement in ISI (b = -1.14, p < 0.001) and PHQ-9 (b = -0.61, p = 0.002) than the control. Critically, the rate of improvement in insomnia symptoms to the last session of treatment, was associated with the subsequent improvement in depressive symptoms post-treatment (b = 2.06, p = 0.017). In contrast, depressive symptom improvement was not associated with insomnia symptom improvement (b = 4.28, p = 0.102).ConclusionThis preliminary data suggests that brief CBTI can reduce pandemic onset insomnia and other depressive symptoms. The preliminary mediation results further suggest that sleep may be an important treatment target for reducing situational depressive symptoms and supports the need to examine the physiological mechanisms of sleep using high-density EEG in a larger sample.Support (if any):

Desynchrony and synchronisation underpinning sleep–wake cycles

This paper studies mechanisms of synchronisation and loss of synchrony among the three key oscillatory processes controlling sleep–wake cycles in the human brain: the 24-h circadian oscillator, the homeostatic sleep drive, and the environmental light–dark cycle. Synchronisation of these three rhythms promotes sleep and brain clearance and is critical for human health. Their desynchrony, on the other hand, is associated with impaired performance and disease development, including cancer, cardiovascular disease, and mental disorders. A biophysical model of arousal dynamics simulating sleep–wake cycles and circadian rhythms is used as the study system. It is based on established neurobiological mechanisms controlling sleep–wake transitions and incorporates the three oscillatory processes. Nonlinear dynamics methods and synchronisation theory are used to numerically investigate model dynamics under conditions that are not easily achievable in experiments. The role of homeostatic brain clearance rate in synchronisation is investigated, and selective turning on and off of coupling strengths between the oscillators allows us to determine their role in oscillators’ dynamics. We find that, in the absence of coupling between the circadian and homeostatic oscillators, the default state of the model corresponds to the endogenous homeostatic period that is far from $$\sim $$ 24-h rhythm of the circadian and light–dark cycles. Combined action of light and circadian oscillator on the homeostatic rhythm is required to achieve the typical sleep–wake pattern that is observed in young healthy people. Under 12-/12-h light–dark conditions with light at 80 lux, change of homeostatic clearance rate is found to induce two types of desynchronisation: (i) fast clearance rates $$\tau _H<58.1$$ h desynchronise the homeostatic oscillator from the circadian, while the circadian rhythm remains entrained to the light–dark cycle, and (ii) slow clearance rates $$\tau _H>69$$ h maintain synchronisation between the homeostatic and circadian oscillators, but the period of both is different from that of the light–dark cycle. Between these regimes, all three rhythms are synchronised under the studied conditions. The model predicts that the system is highly sensitive to external inputs to the neuronal populations of the sleep–wake switch, which affect the endogenous period of the homeostatic oscillator and can lead to complete loss of sleep. Model dynamics show that loss of synchronisation, which is traditionally ascribed solely to impairment of the circadian oscillator, can be caused by changes in the homeostatic clearance rate of the brain or external input to the neuronal populations of the sleep–wake switch. Thus, changes in circadian, homeostatic, and external factors (combined or specific) may be responsible for conditions of desynchronisation. This has significant implications for understanding individual variability in sleep–wake patterns and in mechanisms of sleep and circadian disorders, indicating that both the homeostatic and circadian mechanisms can be responsible for the same clinical or behavioural presentation of a disease.

Exploring and developing the concept of the dream as a threat monitoring-alerting mechanism

Summary. It is not clear that established dream theories adequately explain the purpose of something that accounts for such a substantial percentage of our time. Gewargis’s innovative theory - that dreams function to safeguard the organism during sleep - seems plausible and to have the potential to make an important contribution to a better understanding of why we dream. There are, however, a number of possible problems with it. In particular, the published literature is not used to substantiate the empirical claims upon which the theory is built; and this could be a major issue, as a some of these claims seem to be at variance with current scientific knowledge and/or to have limited face validity. This comment article draws upon the neurology literature to critique and suggest amendments to Gewargis’s theory; and proposes additional hypotheses relating to why and how dreams might act as a monitoring-alerting mechanism and protect the sleeper from a range of internal and external perturbations during REM and NREM sleep; and not just, as Gewargis appears to suggest, guard against inadequate blood flow to the brain or “oxygen-deprivation” to the lungs during REM sleep. A central argument in this comment piece is that to perform a range of functions, such as memory processing, the dream is where the sleeper’s consciousness is focused for much of the time asleep, and so it is also where the alerting-arousal messages need to be presented and processed during that time. In other words, and at variance with what Gewargis proposed, we don’t dream so as to provide a sleep defence mechanism, but a Dream Sleep-Defence Mechanism (DSDM) is needed because we dream. It addition, it argued that dreams - including through the use of broad categories (and, in particular, potential danger/not potential danger), rather than representational reflections of the reality in question - provide a cortical resource efficient mechanism. It is recognised, however, that support for a dream sleep defence mechanism is at best circumstantial and that the idea needs to be tested in experimental studies if it is to move beyond conjecture.

Multi-ancestry genome-wide gene-sleep interactions identify novel loci for blood pressure.

Long and short sleep duration are associated with elevated blood pressure (BP), possibly through effects on molecular pathways that influence neuroendocrine and vascular systems. To gain new insights into the genetic basis of sleep-related BP variation, we performed genome-wide gene by short or long sleep duration interaction analyses on four BP traits (systolic BP, diastolic BP, mean arterial pressure, and pulse pressure) across five ancestry groups in two stages using 2 degree of freedom (df) joint test followed by 1df test of interaction effects. Primary multi-ancestry analysis in 62,969 individuals in stage 1 identified three novel gene by sleep interactions that were replicated in an additional 59,296 individuals in stage 2 (stage 1 + 2 Pjoint < 5 × 10-8), including rs7955964 (FIGNL2/ANKRD33) that increases BP among long sleepers, and rs73493041 (SNORA26/C9orf170) and rs10406644 (KCTD15/LSM14A) that increase BP among short sleepers (Pint < 5 × 10-8). Secondary ancestry-specific analysis identified another novel gene by long sleep interaction at rs111887471 (TRPC3/KIAA1109) in individuals of African ancestry (Pint = 2 × 10-6). Combined stage 1 and 2 analyses additionally identified significant gene by long sleep interactions at 10 loci including MKLN1 and RGL3/ELAVL3 previously associated with BP, and significant gene by short sleep interactions at 10 loci including C2orf43 previously associated with BP (Pint < 10-3). 2df test also identified novel loci for BP after modeling sleep that has known functions in sleep-wake regulation, nervous and cardiometabolic systems. This study indicates that sleep and primary mechanisms regulating BP may interact to elevate BP level, suggesting novel insights into sleep-related BP regulation.

Reducing Network Energy Consumption using Multidimensional Optimization of LEACH Protocol

The optimized LEACH-focused protocol is proposed to make equal network energy usage and outspread the life cycle. In the first place, the threshold function of the cluster head is adjusted and the technique of division of the network area is configured to change reasonably the size of the clusters, taking account of residual energy and node distance. A sleep mechanism is introduced for intra-cluster transmission to balance the power consumption of nodes. And a new Barycenter Node has been introduced to help the head of the cluster fulfill the transmission task and thus prolong the lifespan. We derived a new formula, considering the angle, energy and distance, in multiple-hop communication between clusters to determine the fitting factor of the next hop. The results of simulations display that the remaining total energy of the optimized LEACH is decreased by 32.6% and the network life cycle respectively increases by around 54%.

Development Status of Smart Home System in the Era of Internet of Everything

Driven by the Internet of things technology, the development of smart home is showing a rapid and vigorous development trend. This paper mainly studies the development status of smart home system in the era of Internet of things. After a long time of operation, the system should check the power supply voltage, check whether the LCD display is normal, whether the wireless module can transmit the signal, and whether the signal collected by the sensor is normal. We check all kinds of interfaces and the circuit works normally. After running for a long time, the program checks the working condition of the chip and checks the working state of the chip. The accuracy test environment of this system is the test of air conditioner, TV and socket in the laboratory. Each command word is tested 50 times, and the number of successful experiments is recorded. The data shows that the average transmission time is about 10 ms, and 99.9% of the data transmission delay is less than 30 ms. The results show that the hardware circuit meets the requirements of low-power design, and the embedded software can reduce the system power consumption and achieve business functions through sleep wake-up mechanism.

An energy-saving routing algorithm for opportunity networks based on asynchronous sleeping mode

The opportunistic network is based on the idea of "Store-Carry-Forward" between nodes which haven't complete communication links. It uses the encounter opportunity presented by node mobility to establish a route to realize communication. The traditional Epidemic algorithm uses the flooding mechanism which greatly increases the energy consumption of nodes, and it is often unable to supplement the energy of nodes at any time in the application environment of the opportunistic network. Therefore, this paper proposes an asynchronous sleep mechanism, which allows nodes to judge whether to enter the sleep state according to their own energy situation, real-time state and other information. It ensures that the nodes do not miss the possible communication opportunities by dynamically controlling the sleep time and wake-up time. The simulation results show that the proposed EASE algorithm can guarantee the network performance and greatly reduce the energy consumption of nodes compared with the classical opportunistic network routing algorithms.

Alteration of sleep homeostasis and cognitive impairment in apneic obese adolescents

To evaluate specific features of sleep pattern and neurocognitive performance in OSA obese adolescents to correlate sleep macrostructural parameters and phasic events (K-complexes, KCs; and sleep spindles, SSs) with cognitive functioning in these individuals. Polysomnography was recorded from 25 male apneic obese patients (15–17 years), 20 age- and sex-matched non-apneic obese and 15 lean adolescents. KCs and SSs were identified during stage 2 non-rapid eye movement sleep (N2) and characteristics were evaluated. Furthermore, all participants underwent cognitive performance assessment using a battery of neurocognitive tests. Participant’s data, macro- and microstructural sleep variables and cognitive measures were compared. Finding data were analyzed using descriptive and regression analyses. Differences were reliable at p < 0.05. Compared to both controls, the OSA obese group had significantly reduced sleep onset latency (p = 0.061), slow-wave sleep (SWS) and rapid eye movement (REM) sleep (p < 0.01 for both), but increased N1–N2 stage duration (p < 0.01), the appearance of KCs during apnea and after apnea episodes (DE-KCs and AE-KCs, respectively), reduced spontaneous KCs (SN-KCs) number and periodicity, and lowered amplitude of apnea evoked KCs. SSs activity was an atypical increased in the OSA group. SWS, REM sleep, minimal SaO2, DE-KCs, AE-KCs, and SSs, as well as SN-KCs number, were predictors of cognitive functioning (attention, memory, thinking, speech) changes in OSA adolescents. Together, the above results provide some evidence for impairment in sleep homeostatic mechanisms, when OSA and obesity are comorbid, and provide novel insights into the relationship between sleep microstructure disruption and waking cognitive functioning in these adolescents.

Blue light insertion at night is involved in sleep and arousal-promoting response delays and depressive-like emotion in mice.

Light plays a direct crucial role in the switch between sleep and arousal and the regulation of physiology and behaviour, such as circadian rhythms and emotional change. Artificial lights, which are different from natural light sources with a continuous light spectrum, are composed of three single-colour lights and are increasingly applied in modern society. However, in vivo research on the mechanisms of blue light-regulated sleep and arousal is still insufficient. In this work, we detected the effects of inserting white or blue light for 1 h during the dark period on the wheel-running activity and sucrose preference of C57 mice. The results showed that blue light could induce delays in sleep and arousal-promoting responses. Furthermore, this lighting pattern, including blue light alone, induced depressive-like emotions. The c-fos expression in the blue light group was significantly higher in the arcuate hypothalamic nucleus (Arc) and significantly lower in the cingulate cortex (Cg) and anterior part of the paraventricular thalamic nucleus (PVA) than in the white light group. Compared with the white light group, the phospho-ERK expression in the paraventricular hypothalamic nucleus (PVN) and PVA was lower in the blue light group. These molecular changes indicated that certain brain regions are involved in blue light-induced response processes. This study may provide useful information to explore the specific mechanism of special light-regulated physiological function.

Abstract P68: Disrupted Electrophysiological Sleep in Critically ill Stroke Patients: Does it Matter?

Mounting evidence suggest that poor sleep quality may impact outcome following stroke. While sleep disturbances are common among critically ill patients, little is known about sleep characteristics in neurocritical stroke patients. We examined sleep characteristics in acute stroke patients admitted to an intensive care unit (ICU) compared to those admitted for non-stroke conditions. Methods: Retrospective analysis of critically ill patients who underwent continuous electroencephalographic (cEEG) monitoring in the ICU from 2018-19. Sleep was scored based on American Academy of Sleep Medicine-defined EEG criteria. EEG and clinical characteristics [NIH Stroke Scale (NIHSS), Hunt and Hess (HH) Grade, and ICH Score] were collected. Primary outcomes were based on modified Rankin Scale (mRS) scores of which 2 or less was considered favorable. Differences were assessed using Chi-Square test. Results: 228 ICU patients underwent cEEG; mean age was 58 years (range 18-91) and 57% were male. 61 (27%) were admitted for acute stroke (16 ischemic, 17 aneurysmal subarachnoid hemorrhage (aSAH), 27 non-traumatic intracerebral hemorrhage (ICH)). The other 167 critically ill patients were admitted for medical, surgical, or non-stroke related neurological conditions. In those with stroke, mean NIHSS scores for ischemia, mean ICH Score for ICH, and mean HH for aSAH were 18.78, 2.12, and 3.36, respectively. Rates of attaining any sleep were similar between stroke (27.9%) and non-stroke patients (26.9%). 29.4% of stroke patients who achieved sleep had good outcomes compared to only 9.1% that did not (χ 2 (1)=2.79, p=0.095). In stroke patients that achieved sleep, 52.9% of patients reached Stage N1, 47.1% Stage N2 and none reached Stages N3 or REM. In the non-stroke cohort, 46.6% who achieved sleep had good outcomes compared to 26.2% who did not (χ 2 (1)=6.34, p=0.012). Of these, 37.8% reached Stage N1 sleep, 60% Stage N2, 2.22% Stage N3, and none reached Stage REM. Discussion: Critically ill stroke and non-stroke patients have disrupted electrophysiological sleep, and none reach REM stage. A trend towards improved outcome in stroke survivors was observed in those who slept. The association between sleep variability, stroke mechanism, and functional outcome needs further exploration.

Sleep and circadian rhythm disturbances in intensive care unit (ICU)-acquired delirium: a case-control study.

ObjectiveThe relationships among sleep, circadian rhythm, and intensive care unit (ICU)-acquired delirium are complex and remain unclear. This study aimed to examine the pathophysiological mechanisms of sleep and circadian rhythm disturbances in patients with ICU-acquired delirium.MethodsThis study included critical adult patients aged 18 to 75 years who were treated in the ICU. Twenty-four-hour polysomnography was performed and serum melatonin and cortisol levels were measured six times during polysomnography. Receiver operating characteristic curves and binomial logistic regression were used to evaluate the potential of sleep, melatonin, and cortisol as indicators of delirium in the ICU.ResultsPatients with delirium (n = 24) showed less rapid eye movement (REM) sleep compared with patients without delirium (n = 24, controls). Melatonin levels were lower and cortisol levels were higher in the delirium group than in the control group. REM sleep, melatonin, and cortisol were significantly associated with delirium. The optimal cutoff values of REM sleep and mean melatonin and cortisol levels that predicted delirium were ≤1.05%, ≤422.09 pg/mL, and ≥212.14 ng/mL, respectively.ConclusionsREM sleep, and melatonin and cortisol levels are significantly associated with the risk of ICU-acquired delirium. Improved sleep and readjustment of circadian rhythmicity may be therapeutic targets of ICU-acquired delirium.

Dopamine receptor DOP-1 engages a sleep pathway to modulate swimming in C. elegans

SummaryAnimals require robust yet flexible programs to support locomotion. Here we report a pathway that connects the D1-like dopamine receptor DOP-1 with a sleep mechanism to modulate swimming in C. elegans. We show that DOP-1 plays a negative role in sustaining swimming behavior. By contrast, a pathway through the D2-like dopamine receptor DOP-3 negatively regulates the initiation of swimming, but its impact fades quickly over a few minutes. We find that DOP-1 and the GPCR kinase (G-protein-coupled receptor kinase-2) function in the sleep interneuron RIS, where DOP-1 modulates the secretion of a sleep neuropeptide FLP-11. We further show that DOP-1 and FLP-11 act in the same pathway to modulate swimming. Together, these results delineate a functional connection between a dopamine receptor and a sleep program to regulate swimming in C. elegans. The temporal transition between DOP-3 and DOP-1 pathways highlights the dynamic nature of neuromodulation for rhythmic movements that persist over time.

Research of Multidimensional Optimization of LEACH Protocol Based on Reducing Network Energy Consumption

In order to equalize network energy consumption, and extend the life cycle, the optimized protocol based on low-power adaptive cluster stratification (LEACH) is proposed. Firstly, considering residual energy and distance of nodes, the threshold function of the cluster head is modified, and the network region division strategy is optimized, to reasonably adjust the size of clusters. For intracluster transmission, a sleep mechanism is added to balance node energy consumption. And a new barycenter node is added to assist cluster head (CH) to complete the transmission task, thereby extending the service lifetime. In the multihop communication between clusters, in order to calculate the fitting factor of the next hop, we derived a new formula, which takes into account the angle, remaining energy, and distance. Simulation results show that the total remaining energy of the optimized LEACH protocol is reduced by 31.4%, and the network life cycle is increased by about 52%.

Past, present, and future of sleep medicine research in Latin America.

Sleep medicine is a relatively young field with exponential growth in development and research in the last decades. Parallel to the advances in the United States, Latin America also had its beginnings in sleep medicine housed in neuroscience laboratories. Since the very first Latin American meeting in 1985, and the first sleep society in 1993, sleep research has undergone significant development in subsequent years. From contributions in animal research that allowed understanding of the activity of the brain during sleep to the studies that improved our knowledge of sleep disorders in humans, Latin America has become a scientific hub for expansion of sleep research. In this article, we present a historical account of the development of sleep medicine in Latin America, the current state of education and the achievements in research throughout history, and the latest advances in the trending areas of sleep science and medicine. These findings were presented during World Sleep Society meeting in Vancouver in 2019 and complement the work on sleep societies and training published by Vizcarra-Escobar et al in their article "Sleep societies and sleep training programs in Latin America" (J Clin Sleep Med. 2020;16(6):983-988).

Performance Optimization of Cloud Data Centers with a Dynamic Energy-Efficient Resource Management Scheme

As an advanced network calculation mode, cloud computing is becoming more and more popular. However, with the proliferation of large data centers hosting cloud applications, the growth of energy consumption has been explosive. Surveys show that a remarkable part of the large energy consumed in data center results from over-provisioning of the network resource to meet requests during peak demand times. In this paper, we propose a solution to this problem by constructing a dynamic energy-efficient resource management scheme. As a way of saving energy as well as maintaining cloud user’s quality of experience, the scheme presents a multitier cloud architecture by configuring physical machines (PMs) into two pools: a hot (running) pool and a warm (turned on, but in dynamic sleep) pool. Each PM is configured with a resource search engine (RSE) that finds an available virtual machine (VM) for the request, and a synchronous sleep mechanism is introduced to the warm pool. To analyze the end-to-end performance of the cloud system’s service with the proposed scheme, we establish a hybrid queueing system composed of three stochastic submodels by using a matrix-geometric solution. Accordingly, the average latency of requests and the energy-saving rate of the system are derived. Through numerical results, we show the influence of the synchronous sleep mechanism on the system performance. Moreover, from the perspective of economics, we build a system cost function to study the trade-off between different performance measures. An improved Salp Swarm Algorithm (SSA) is presented to minimize the system cost and optimize the sleep parameter.

Does sleep flush wastes from the brain?

. Does sleep flush wastes from the brain? Sleep is vital across all species, and sleep deprivation has detrimental consequences for the organism. Sleep, but not wakefulness, seems to allow removal of waste metabolites from the brain, clearing the brain from the potential neurotoxic waste products that accumulate during wakefulness. The wastes are removed by cerebrospinal fluid transport, the 'glymphatic system', named after its dependence on the glia, and the resemblance with the lymphatic system in peripheral tissues. A brief synthesis of the new discoveries and their implications for the understanding of sleep functions and mechanisms is presented.

Neurobiology of sleep (Review)

Sleep is a physiological global state composed of two different phases: Non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. The control mechanisms of sleep manifest at the level of genetic, biological and cellular organization. Several brain areas, including the basal forebrain, thalamus, and hypothalamus, take part in regulating the activity of this status of life. The signals between different brain regions and those from cortical areas to periphery are conducted through various neuromediators, which are known to either promote wakefulness or sleep. Among others, serotonin, norepinephrine, histamine, hypocretin (orexin), acetylcholine, dopamine, glutamate, and gamma-aminobutyric acid are known to orchestrate the intrinsic mechanisms of sleep neurobiology. Several models that explain the transition and the continuity between wakefulness, NREM sleep and REM sleep have been proposed. All of these models include neurotransmitters as ligands in a complex reciprocal connectivity across the key-centers taking part in the regulation of sleep. Moreover, various environmental cues are integrated by a central pacemaker-located in the suprachiasmatic nucleus-which is able to connect with cortical regions and with peripheral tissues in order to promote the sleep-wake pattern.

Sleep-Dependent Directional Interactions of the Central Nervous System-Cardiorespiratory Network.

We investigated the nature of interactions between the central nervous system (CNS) and the cardiorespiratory system during sleep. Overnight polysomnography recordings were obtained from 33 healthy individuals. The relative spectral powers of five frequency bands, three ECG morphological features and respiratory rate were obtained from six EEG channels, ECG, and oronasal airflow, respectively. The synchronous feature series were interpolated to 1 Hz to retain the high time-resolution required to detect rapid physiological variations. CNS-cardiorespiratory interaction networks were built for each EEG channel and a directionality analysis was conducted using multivariate transfer entropy. Finally, the difference in interaction between Deep, Light, and REM sleep (DS, LS, and REM) was studied. Bidirectional interactions existed in central-cardiorespiratory networks, and the dominant direction was from the cardiorespiratory system to the brain during all sleep stages. Sleep stages had evident influence on these interactions, with the strength of information transfer from heart rate and respiration rate to the brain gradually increasing with the sequence of REM, LS, and DS. Furthermore, the occipital lobe appeared to receive the most input from the cardiorespiratory system during LS. Finally, different ECG morphological features were found to be involved with various central-cardiac and cardiac-respiratory interactions. These findings reveal detailed information regarding CNS-cardiorespiratory interactions during sleep and provide new insights into understanding of sleep control mechanisms. Our approach may facilitate the investigation of the pathological cardiorespiratory complications of sleep disorders.

Even a Mild Sleep Restriction Can Impact Daytime Functioning in Children with ADHD and Their Typically Developing Peers

ABSTRACT Objectives/Background Correlational studies show that short sleep is associated with negative daytime outcomes in school-aged children, but there are few experimental sleep manipulation studies to assess whether this is a causal relation. The aim of this study was to determine the impact of mild, cumulative sleep restriction on daytime functioning of typically developing (TD) children and children with attention-deficit/hyperactivity disorder (ADHD). Participants A total of 36 school-aged children (n = 18 TD; n = 18 ADHD), aged 6–11 years participated. Methods Children participated in two sleep conditions (order counter-balanced). The Restricted condition required a 1 h reduction of time in bed for one week, and the Controlled Typical condition was based on participant’s average baseline sleep. At the end of each condition, participants attended the sleep lab for overnight polysomnography and daytime functioning assessments. Results Children successfully reduced time in bed by ~1 h. Due to compensatory changes, total sleep time (TST) was reduced by only ~20 min, as children fell asleep faster and spent less time awake after sleep onset during the Restricted compared to Controlled Typical condition. Many daytime functions were not affected by this very mild sleep restriction, however, both groups showed significant changes in performance on an objective attention task and on a parent-rated emotional lability measure after six nights of minimal reductions in TST. There were no significant differences between groups. Conclusions Results suggest that a very mild sleep restriction can affect children’s attention and emotional regulation, even with evidence of compensatory sleep mechanisms.